The present invention is related to methods and apparatus for surgically implantable pumps that provide a mechanical device for augmenting or replacing the blood pumping action of damaged or diseased hearts. More specifically, this invention is related to methods and apparatus for conduits for such pumps to meet the three-fold requirements of a substantially non-delaminable conduit having a highly non-thrombogenic porous inner surface that is not susceptible to air leakage under negative pressure, whereby the use of such implantable pump procedures is broadly enabled, and wherein the functional utility, ease of use, and wide applicability of the device in medical practice constitutes progress in science and the useful arts. Furthermore, the present invention teaches processes to make and use the device in medical practice.
Of all the cardiovascular disorders, congestive heart failure (CHF) is the only one to show a sharp increase in prevalence since the 1960s. This rise in the number of cases of CHF worldwide is a major and growing public health concern. While the prevalence of coronary heart disease (CHD) has declined in the past few decades and the prevalence of stroke has remained steady until recent years, the number of people suffering from CHF has increased dramatically. In terms of mortality and morbidity, the prognosis for CHF is depressingly poor and in the US, the disease has been recognized as ‘epidemic’. The high costs associated with the condition will place an added burden on public health resources as the incidence of CHF continues to rise.
By definition, CHF is a disorder in which the heart fails to pump blood adequately to other organs in the body. This can result in a shortness of breath, fatigue and fluid retention (edema) and if left unchecked can lead to death within a few years. CHF is not a disease per se but a condition that arises as a result of various cardiovascular diseases (CVD). In effect, CHF is the end-stage syndrome of heart muscle disorders and diseases such as hypertension and CHD, which can damage or impair the functionality of the heart and the vessels supplying it.
In the majority of cases, CHF is a progressive condition and over time, the ability of the heart muscle to function properly deteriorates—this process is called cardiac remodeling. As the condition worsens, the ventricular muscle over-stretches and the muscle fails to work to its full efficiency. This leads to a further reduction in the cardiac output and exacerbates symptoms of heart failure.
In CHF, the reduced cardiac output causes a fall in arterial pressure leading to the activation of several compensatory reflexes. The sympathetic nervous system is stimulated, resulting in a direct increase in the force of contraction of the heart and a greater venous return as a response to venoconstriction. Long-term compensation includes the activation of the renin angiotensin system (RAS) and subsequent renal fluid retention. The combined effect of these responses can lead to the formation of edema, especially in the legs and ankles. If heart failure occurs in the left side of the heart, pulmonary edema can result which manifests as breathlessness. In advanced CHF, the severity of the symptoms can be disabling and often leads to hospitalization. An added consideration is sudden cardiac death, which can occur at any time during the course of CHF.
The most common classification of CHF is based on criteria set out by the New York Heart Association (NYHA). Originally published in 1928, the classifications defined the stages of CHF by its clinical severity and the functional status of the cardiac muscle. Over the years the classifications have been updated and the latest revision was in 1994. The NYHA classes of CHF are listed below.